A High-Fat Diet Expands Body Fat Mass and up-Regulates Expression of Genes Involved in Adipogenesis and Inflammation in a Genetically Lean Pig

Background: Pigs have been proved to be desirable models in studying obesity/adiposity as of their (patho-)physiological similarity to humans. The present study aimed to explore the possibility and characteristics of diet-induced obesity/adiposity in genetically lean pigs.

Methods: Crossbred pigs (Duroc-Landrace × Yorkshire; n = 112; male) were fed a control (4% fat, 13.38 MJ/kg feed) or a high-fat (HF, 11.4% fat, 15.55 MJ/kg feed) diet for 3 months. Body weight, feed intake, and dorsal fat thickness were recorded. Body composition and dorsal fat histology were evaluated. An Automatic Biochemical Analyzer measured plasma lipids and glucose, radioimmunoassays determined plasma insulin, leptin, triiodothyronine, thyroxine, and growth hormone levels, and microarray analysis evaluated gene expression profiles in dorsal fat.

Results: Approximately 70% of the pigs fed HF diet developed obesity. Body weight and energy intake did not differ between control and diet-induced obese (DIO) pigs. Fat mass percentage, adipocyte size, plasma lipids, insulin, and leptin concentrations were significantly higher in DIO pigs than controls. HF diet significantly regulated the expression of 576 genes. Of these, 108 genes were involved in 21 pathways, with 20 genes related to adiposity development and 26 to immune responses.

Conclusions: The genetically lean pigs were observed for the first time to be induced into obesity/adiposity under a HF diet with body fat mass expansion and adipose-related inflammation.